The mitochondrial Ca2+ uniporter MCU is essential for glucose-induced ATP increases in pancreatic β-cells.

Stimulation with LTC4 induced a substantial increase in the number of GFP-positive cells (Figure 5B) and this was significantly reduced both by mitochondrial depolarisation (Figure

Furthermore, decreased ATP synthesis that results from mitochondrial dysfunction also plays an impor- tant role in decreasing insulin secretion in patients with DM2, since it

In the present report, we show that com- pound 48/80 also inhibits glucose-induced PI turn- over and that the PLC1 encoded phospholipase C is essential both for glucose-induced

In β cells, the UCP2 protein is known to inhibit insulin secretion by routing glucose metabolism toward a molecule called NADH, rather than toward ATP. The authors demonstrate

MB significantly increases mitochondrial complex I–III activity in isolated mitochondria and enhances oxygen consumption and glucose uptake in HT-22 cells.. Using positron

As a consequence of this increased inner mitochondrial perme- ability to protons, part of the energy stored as membrane potential generated by the mito- chondrial respiratory chain

The glucose or galactose-grown yeast cells present differ- ences in the cytosolic calcium levels that were attributed to the differences in the internal level of glucose-6-P and Fig.

These results indicate that the higher cytosolic Ca 2 + level in activated lymphocytes increases their susceptibility to oxidative stress-induced cell death in a mechanism involving